A state of immunosuppression has been demonstrated to occur in a malaria infection. The immunosuppression appears to be essentially humoral and not cellular since the classical lymphocyte-mediated cellular immune responses are normal. For this reason, it has been suggested that the suppressed immune response is secondary to macrophage dysfunction. It is the purpose of this research proposal to determine what aspect of of macrophage function is impaired in a malaria function. In vitro and in vivo experiments will be undertaken to demonstrate the ability of hepatic, splenic and peritoneal macrophage of normal and malaria infected mice to phagocytize an antigen and to produce an immunogenic fraction capable of inducing an immune response, as evaluated by the production of circulating antibody and splenic plaque- formation, when transferred to normal mice. Preliminary investigations have demonstrated that peritoneal macrophages from normal mice incubated with antigen are capable of evoking an immune response when transferred to either normal or malaria infected mice. However, transfer of peritoneal macrophages from malaria infected mice incubated with antigen to either normal or malaria infected mice did not elicit such a response. These results suggest a malaria induced impairment in macrophage antigen processing mechanisms. Since an enhanced susceptibility to bacterial infections has been demonstrated in malaria, an impaired bactericidal activity of macrophages has also been predicated. The bactericidal activity of macrophages from malaria infected mice will, therefore, be examined.